Ingrosso D, D'Angelo S, Perrotta S, d'Urzo G, Iolascon A, Perna A F, Galletti P, Zappia V, Miraglia del Giudice E
Institute of Biochemistry of Macromolecules, Second University of Naples, Italy.
Br J Haematol. 1996 Apr;93(1):38-41. doi: 10.1046/j.1365-2141.1996.451990.x.
Based on quantitative analysis of red cell membrane proteins, hereditary spherocytosis (HS) can be divided into two main groups including isolated or ankyrin combined spectrin deficiency and band 3 reduction. Protein methyl esterification catalysed by protein carboxyl methyl-transferase (PCMT type II; EC 2.1.1.77) is a post-biosynthetic modification which is involved in the metabolism of damaged membrane proteins. We utilized the evaluation of erythrocyte membrane protein methyl esterification as a marker of cytoskeletal disarray in seven HS subjects with spectrin reduction and in seven patients with HS due to band 3 deficiency. Our results support the notion that band 3 deficient erythrocytes are not affected by an extensive cytoskeletal derangement. On the contrary, we found a remarkable increase of membrane methylation in the unsplenectomized, spectrin-deficient. HS patients, suggesting a striking membrane skeleton disarray. This phenomenon was not observed in the spectrin-deficient red cells of splenectomized patients. Therefore in spectrin deficient erythrocytes the induction of cytoskeletal damage, specifically recognized by PCMT type II, could be one of the splenic steps producing conditioned spherocytes.
基于对红细胞膜蛋白的定量分析,遗传性球形红细胞增多症(HS)可分为两个主要组,包括孤立的或锚蛋白联合血影蛋白缺乏以及带3减少。由蛋白质羧基甲基转移酶(II型PCMT;EC 2.1.1.77)催化的蛋白质甲基酯化是一种生物合成后修饰,参与受损膜蛋白的代谢。我们将红细胞膜蛋白甲基酯化评估作为细胞骨架紊乱的标志物,对7例血影蛋白减少的HS患者和7例因带3缺乏导致HS的患者进行了研究。我们的结果支持这样一种观点,即带3缺乏的红细胞不受广泛细胞骨架紊乱的影响。相反,我们发现未行脾切除术、血影蛋白缺乏的HS患者的膜甲基化显著增加,提示明显的膜骨架紊乱。在脾切除患者的血影蛋白缺乏的红细胞中未观察到这种现象。因此,在血影蛋白缺乏的红细胞中,由II型PCMT特异性识别的细胞骨架损伤的诱导可能是产生条件性球形红细胞的脾脏步骤之一。